Dietary deficiency of phosphorus ,calcium ,vitamin D and imbalance
of the calcium :phosphorus ratio
A dietary deficiency or disturbance in the metabolism of calcium,
phosphorus, or vitamin D, including imbalance of the calcium:
phosphorus ratio, is the principal cause of the osteodystrophies. The
interrelation of these various factors is often very difficult to define and
because the end result in all these deficiencies is so similar the precise
etiological agent is often difficult to determine in any given
circumstance.
Absorption and metabolism of calcium and phosphorus
In ruminants, dietary calcium is absorbed by the small intestine according
to body needs.
Calcium absorption is increased in adult animals during periods of high
demand, such as pregnancy and lactation, or after a period of calcium
deficiency, but a substantial loss of body stores of calcium appears to be
necessary before this increase occurs.
The dietary factors influencing the efficiency of absorption of calcium
include the nature of the diet, the absolute and relative amounts of
calcium and phosphorus present in the diet and the presence of interfering
substances. Phosphorus is absorbed by young animals from both milk and
forage-containing diets with a high availability (80-1 00%), but the
availability is much lower (50- 60%) in adult animals .
The metabolism of calcium and phosphorus is influenced by the
parathyroid hormone calcitonin and vitamin D. Parathyroid hormone is
secreted in response to hypocalcemia and stimulates the conversion
of 25 -dihydroxy cholecalciferol to 1,25 -dihydroxy cholecalciferol (1,25DHCC). Parathyroid hormone and 1,25- DHCC together stimulate bone
re sorption and 1,25-DHCC alone stimulates intestinal absorption of
calcium. Calcium enters the blood from bone and intestine, and when
the serum calcium level increases above normal, parathyroid hormone is
inhibited and calcitonin secretion stimulated. The increased calcitonin
concentration blocks bone re sorption and the decreased parathyroid
hormone concentration depresses calcium absorption.
Calcium deficiency (hypocalcicosis)
Calcium deficiency may be primary or secondary, but in both cases, the
end result is an osteodystrophy, the specific disease depending largely on
the species and age of the animals affected.
Etiology
A primary deficiency due to a lack of calcium in the diet is uncommon,
although a secondary deficiency due to a marginal calcium intake
aggravated by a high phosphorus intake is not uncommon. In ponies, such
a diet depresses intestinal absorption and retention of calcium in the body
and the re sorption of calcium from bones is increased.
Epidemiology
Calcium deficiency is a sporadic disease occurring in particular groups of
animals rather than in geographically limited areas. Although death does
not usually occur, there may be considerable loss of function and
disabling lesions of bones or joints. Horses in training, cattle being fitted
for shows, and valuable stud sheep are often fed artificial diets containing
cereal or grass hays which contain little calcium and grains which have a
high content of phosphorus. The secondary calcium deficiency that
occurs in these circumstances is often accompanied by a vitamin D
deficiency because of the tendency to keep animals confined indoors.
Dairy cattle may occasionally be fed similarly imbalanced diets, the
effects of which are exaggerated by high milk production.
Outbreaks can affect many sheep and are usually seen in winter and
spring, following exercise or temporary starvation. In most outbreaks the
characteristic osteoporosis results from a long-term deprivation of food
due to poor pasture growth.
In females there is likely to be a cycle of changes in calcium balance, a
negative balance occurring in late pregnancy and early lactation and a
positive balance in late lactation and early pregnancy and when lactation
has ceased. The negative balance in late pregnancy is in spite of a
naturally occurring increased absorption of calcium from the intestine at
that time, at least in ewes.
Pathogenesis
The main physiological functions of calcium are the formation of bone
and milk, participation in the clotting of blood and the maintenance of
neuromuscular excitability.
In the development of osteodystrophies, dental defects and tetany the role
of calcium is well understood but the relation between deficiency of the
element and lack of appetite, poor growth, loss of condition, infertility
and reduced milk flow is not readily apparent. The disinclination of the
animals to move about and graze and poor dental development may
contribute to these effects.
Feeding repletion diets results in complete remineralization of rib bones,
but only partial remineralization of the metatarsal bones.
Nutritional factors other than calcium, phosphorus and vitamin D may be
important in the production of osteodystrophies, which also occur in
copper deficiency, fluorosis and chronic lead poisoning. Vitamin A is
also essential for the development of bones, particularly those of the
cranium.
Clinical findings
●the clinical findings are less marked in adults than in young animals, in
which there is decreased rate or cessation of growth and dental mal
development.
●The deformity of the gums, poor development of the incisors, failure of
permanent teeth to erupt for periods of up to 27 months and abnormal
wear of the permanent teeth due to defective development of dentine and
enamel, occurring principally in sheep.
● A calcium deficiency may occur in lactating ewes and sucking lambs
whose metabolic requirements for calcium are higher than in dry and
pregnant sheep.
●Exercise and fasting often precipitate tetanic seizures and parturient
paresis in such sheep.
●Attention is drawn to the presence of the disease by the occurrence of
tetany, convulsions and paresis but the important signs are ill-thrift.
●Serum calcium levels will be as low as 5.6 mg/dL (1.4 mmol/L) .
●There is lameness, but fractures are not common even though the bones
are soft.
●A simple method for assessing this softness is compression of the
frontal bones of the skull with the thumbs. In affected sheep, the bones
can be felt to fluctuate.
● In appetence, stiffness, tendency of bones to fracture, disinclination to
stand, difficult parturition, reduced milk flow, loss of condition, and
reduced fertility are all non-specific signs recorded in adults. all nonspecific signs recorded in adults.
●Specific syndromes
Primary calcium deficiency no specific syndromes are recorded.
Secondary calcium deficiency Rickets, osteomalacia, osteodystrophia
fibrosa of the horse and pig and degenerative arthropathy of cattle are the
common syndromes in which secondary calcium deficiency is one of the
specific causative factors. In sheep, rickets is seldom recognized, but
there are marked dental abnormalities.
Clinical pathology
Data on serum calcium and phosphorus and plasma phosphatase levels,
radiographical examination of bones and balance studies of calcium and
phosphorus retention are all of value in determining the presence of
osteodystrophic disease, but determination of the initial causative factor
will still depend on analysis of feedstuffs and comparison.
The response to dietary supplementation with calcium is also of
diagnostic value.
Necropsy findings
True primary calcium deficiency is extremely rare but when it does occur,
severe osteoporosis and parathyroid gland hypertrophy are the significant
findings.
The cortical bone is thinned and the metaphyseal trabeculae appear
reduced in size and number. The ash content of the bone is low because
the bone is resorbed before it is properly mineralized.
Calcium deficiency secondary to other nutritional factors is common and
typically induces the from of osteodystrophy known as osteodystrophia
fibrosa. In most instances, the confirmation of a diagnosis of
hypocalcinosis at necropsy includes an analysis of the diet for calcium,
phosphorus, and vitamin D content.
Treatment and Control
The response to treatment is rapid and the preparations and doses
recommended below are effective as treatment. Parenteral injections of
calcium salts are advisable when tetany is present. When animals have
been exposed to dietary depletion of calcium and phosphorus over a
period of time, it is necessary to supplement the diet with calcium and
phosphorus during dietary mineral repletion.
The provision of adequate calcium in the diet, the reduction of
phosphorus intake where it is excessive and the provision of adequate
vitamin D are the essentials of both treatment and prevention.
Phosphorus deficiency (hypophosphatosis)
Phosphorus deficiency is usually primary and is characterized by pica,
poor growth, infertility and, in the later stages, osteodystrophy.
Hypophosphatemia in dairy cattle is also associated with increased
fragility of red blood cells and post parturient hemoglobinuria.
Etiology
Phosphorus deficiency is usually primary under field conditions but may
be exacerbated by a deficiency of vitamin D and possibly by an excess of
calcium.
Epidemiology
Primary phosphorus deficiency occurs worldwide. Soils and crops
commonly deficient in phosphorus. Primary deficiency may occur in
lactating dairy cattle in early lactation. Occurs under range conditions in
beef cattle and sheep.
In pigs not supplemented with sufficient phosphorus.
Pathogenesis
From 80 to 85 % of the phosphorus of the body is located in the skeleton
where it occurs as hydroxyapatite in a 1.0:1.7 ratio with calcium. These
two minerals provide bone strength necessary for normal activities, such
as grazing. Bone phosphorus also functions as an important phosphorus
reservoir for re sorption when body requirements temporarily exceed
dietary intake.
Phosphorus is also essential for a broad range of enzymatic reactions,
especially those concerned with energy metabolism and transfer.
Phosphorus is also essential for the transfer of genetic information and is
a vital component of various buffering systems.
Phospholipids are necessary for maintenance of cell wall structure and
Prolonged phosphorus deficiency was associated with increased plasma
concentrations of total calcium and 1,25- dihydroxyvitamin D and
reduced plasma concentrations of parathyroid hormone.
Rumen microbes have a phosphorus requirement apart from the animals
requirement which must be met for optimum rumen microbial activity to
occur .phosphorus is essential for the laying down of adequately
mineralized bones and teeth and a deficiency will result in their abnormal
development . Inorganic phosphate which may be ingested as such, or
liberated from esters during digestion or in intermediary metabolism, is
utilized in the formation of proteins and tissue enzymes and is withdrawn
from the plasma inorganic phosphate for this purpose. Experimentally,
female beef cattle fed diets containing <6 g of phosphorus/day developed
an insidious and subtle complex syndrome characterized by weight loss,
rough hair coat, abnormal stance, and lameness Spontaneous fractures
occurred in the vertebrae, pelvis, and ribs. Some affected bones were
severely demineralized and the cortical surfaces were porous, chalky
white, soft, and fragile. The osteoid tissue was not properly mineralized.
Experimental acute depletion of phosphorus in cattle results in a marked
decline in serum inorganic phosphorus and affected animals display an
avid appetite for old bones The signs include: Failure to gain weight and
maintain body condition, Reduced bone weight ,Osteopenia
radiographically ,and Evidence of reduced bone formation.
Clinical findings
Primary phosphorus deficiency is common only in cattle. Young animals
grow slowly and develop rickets. In adults there is an initial subclinical
stage followed by osteomalacia.
In cattle of all ages a reduction in voluntary intake of feed is a first effect
of phosphorus deficiency and is the basis of most of the general systemic
signs.
Retarded growth, low milk yield, and reduced fertility are the earliest
signs of phosphorus deficiency.
In severe phosphorus deficiency in range beef cattle, the calving
percentage has been known to drop from 70 to 20 % .
Although it is claimed that relative infertility occurs in dairy heifers on
daily intakes of less than 40 g of phosphate, the infertility being
accompanied by anestrus, sub estrus, and irregular estrus and delayed
sexual maturity this has not been borne out by other experimental work,
which indicates that fertility is independent of the calcium or phosphorus
content or the calcium :phosphorus ratio of the diet in cattle.
In the experimental production of phosphorus deficiency in beef cows,
The clinical signs included general un thriftiness, marked body weight
loss, reduced feed consumption, reluctance to move, abnormal stance,
bone fractures, and finally impaired reproduction.
The detectable signs of phosphorus deficiency developed in the following
sequence:
-Loss of body weight and condition
-Decreased whole blood phosphorus associated with increased whole
blood calcium concentration
-Allotriophagia
-Abnormal stance, locomotion and recumbence.
In a severely deficient area, a characteristic conformation develops and
introduced cattle revert to the district type in the next generation.
The animals have a leggy appearance with a narrow chest and small girth,
the pelvis is small, and the bones are fine and break easily.
The chest is slabsided due to weakness of the ribs and the hair coat is
rough and staring and lacking in pigment. In areas of severe deficiency,
the mortality rate may be high due to starvation, especially during periods
of drought when deficiencies of phosphorus, protein and vitamin A are
exaggerated.
Osteophagia is common and may be accompanied by a high incidence of
botulism. Cows in late pregnancy often become recumbent and, although
they continue to eat, are unable to rise.
Acute recumbency in high-producing dairy cows on a marginally
phosphorus deficient diet may become recumbent in early lactation.
Affected animals are recumbent and cannot stand. They may be bright
and alert and their vital signs are within normal range.
Although sheep and horses it phosphorus-deficient areas do not develop
clinically apparent osteodystrophy they are often of poor stature and
unthrifty and may develop perverted appetites. An association between
low blood phosphorus and infertility in mares has been suggested but the
evidence is not conclusive.
Clinical pathology
Serum phosphorus
Blood levels of phosphorus are not a good indicator of the phosphorus
status of an animal because they can remain at normal levels for long
periods after cattle have been exposed to a serious deficiency of the
element.
Generally, clinical signs occur when blood levels have fallen from the
normal of 4-5 mg/dL (1.3-1.7 mmol/L) to 1.5-3.5 mg/dL (0.5-1.2 mmolL)
and a response to phosphate supplementation in body weight gain can be
anticipated in cattle that have blood inorganic phosphorus levels of less
than 4 mg/dL(1.3 mmol/L).Levels may fall as low as1mg/dL(0 3 mmolL)
or less in severe clinical cases.
Phosphorus content of diet
Estimation of the mineral content in pasture and drinking water is a
valuable aid in diagnosis. A technique has been devised for determining
phosphorus intake of sheep by estimating the phosphorus content of
feces.
Bone ash concentrations
Determination of total bone ash concentrations and bone calcium and
phosphorus concentrations from sample of rib can provide useful
diagnostic information and comparison to normal values.
Differential diagnosis
osteomalacia.
Those
diseases
resembling
rickets
and
Treatment
The preparations and doses recommended under control can be
satisfactorily used for the treatment of affected animals. In cases where
the need for phosphorus is urgent, as in postparturient hemoglobinuria
and in cases of parturient paresis complicated by hypophosphatemia, the
intravenous administration of sodium acid phosphate (30 g in 300 mL
distilled water) is recommended.
Control Supplement diets with adequate phosphorus, calcium, and
vitamin D.
Tox icity of supplements
The use of phosphate supplements in the diet is not without hazards.
Phosphoric acid is directly toxic and should not be used and monosodium
phosphate is unpalatable to many animals; the depression of appetite that
results may discount the improved feed utilization it provides.
Superphosphate used as fertilizer can cause toxicosis in ruminants
Clinical signs in sheep include teeth grinding, diarrhea, nervous system
depression, apparent blindness, stiffness ,and ataxia and high fatality rate.
Vitamin D deficiency
Vitamin D deficiency is usually caused by insufficient solar irradiation of
animals or their feed and is manifested by poor appetite and growth and
in advanced cases by osteodystrophy.
Etiology
A lack of ultraviolet solar irradiation of the skin, coupled with a
deficiency of preformed vitamin D complex in the diet, leads to a
deficiency of vitamin D in tissues.
Epidemiology Uncommon because diets are supplemented. Occurs in
animals in countries with relative lack of UV irradiation especially in
winter months; animals raised in doors for long periods.
May occur in young grazing animals in winter months. May be
antivitamin D factor.
Pathogenesis
Vitamin D is a complex of substances with anti-rachitogenic activity. The
important components are as follows:
- Vitamin D3 (cholecalciferol) is produced from its precursor 7 dehydrocholesterol in mammalian skin and by natural irradiation with
ultraviolet light.
- Vitamin D2 is present in sun-cured hay and is produced by ultraviolet
irradiation of plant sterols. Calciferol or viosterol is produced
commercially by the irradiation of yeast. Ergosterol is the provitamin.
- Vitamin D4 and Ds occur naturally in the oils of some fish.
Vitamin D produced in the skin or ingested with the diet and absorbed by
the small intestine is transported to the liver. In the liver, 25hydroxycholecalciferol is produced, which is then transported to the
kidney where at least two additional derivatives are formed by 1-αhydroxylase.
One is 1,25- dihydroxycholecalciferol (DHCC) and the other is 24,25DHCC.
Under conditions of calcium need or calcium deprivation the form
predominantly produced by the kidney is 1,25- DHCC. At present, it
seems likely that 1,25-DHCC is the metabolic form of vitamin D most
active in eliciting intestinal calcium transport and absorption and is
at least the closest known metabolite to the form of vitamin D functioning
in bone mineralization.
The metabolite also functions in regulating the absorption and
metabolism of the phosphate ion and especially its loss from the kidney.
A deficiency of the metabolite may occur in animals with renal disease,
resulting in decreased absorption of calcium and phosphorus, decreased
mineralization of bone, and excessive losses of the minerals through the
kidney.
A deficiency of vitamin D per se is governed in its importance by the
calcium and phosphorus status of the animal.
Because of the necessity for the conversion of vitamin D to the active
metabolites, there is a lag period of 2-4 days following the administration
of the vitamin parenterally before a significant effect on calcium and
phosphorus absorption can occur.
The use of synthetic analogs of the active metabolites such as 1 - αhydroxycholecalciferol (an analog of 1,25-DHCC) can increase the
plasma concentration of calcium and phosphorus within 12 h following
administration and has been recommended for the control of parturient
paresis in cattle.
Maternal status
Maternal vitamin D status is important in determining neonatal plasma
calcium concentration. There is a significant correlation between
maternal and neonatal calf plasma concentrations of vitamin D. This
indicates that the vitamin D metabolite status of the neonate is primarily
dependent on the vitamin D status of the dam . The maternal serum
concentrations of calcium, phosphorus, and magnesium do not determine
concentrations of these minerals found in the newborn calf.
The ability of the placenta to maintain elevated plasma calcium or
phosphorus in the fetus is partially dependent on maternal 1,25- (OH)2 D
status.
Calcium : phosphorus ratio
When the calcium: phosphorus ratio is wider than the optimum (1:1 to
2:1), vitamin D requirements for good calcium and phosphorus retention
and bone mineralization are increased. A minor degree of vitamin D
deficiency in an environment supplying an imbalance of calcium and
phosphorus might well lead to disease, whereas the same degree of
vitamin deficiency with a normal calcium and phosphorus intake could go
unsuspected.
The minor functions of the vitamin include maintenance of efficiency of
food utilization and a calorigenic action, the metabolic rate being
depressed when the vitamin is deficient. These actions are probably the
basis for the reduced growth rate and productivity in vitamin D
deficiency.
Some evidence suggests that vitamin D may have a role in the immune
system.
Clinical findings
1-The most important effect of lack of vitamin D in farm animals is
reduced productivity.
2-A decrease in appetite and efficiency of food utilization cause poor
weight gains in growing stock and poor productivity in adults.
Reproductive efficiency is also reduced and the overall effect on the
animal economy may be severe.
3-In the late stages lameness, which is most noticeable in the forelegs, is
accompanied in young animals by bending of the long bones and
enlargement of the joints.
4-The latter stage of clinical rickets may occur Simultaneously with
cases of osteomalacia in adults.
5- An adequate intake of vitamin D appears to be necessary for the
maintenance of fertility in cattle, particularly if the phosphorus intake is
low.
Clinical pathology
Serum calcium and phosphorus
A pronounced hypophosphatemia occurs in the early stages and is
followed some months later by a fall in serum calcium.
Plasma alkaline phosphatase levels are usually elevated. The blood
picture quickly returns to normal with treatment.
Plasma vitamin D
The normal ranges of plasma concentrations of vitamin D and its
metabolites in the farm animal species are now available and can be used
to monitor the response of the administration of vitamin D parenterally or
orally in sheep. The serum concentrations of vitamin D in the horse have
been determined.
Necropsy findings
The pathological changes in young animals are those of rickets, while in
older animals there is an osteomalacia.
In all ages, a variable amount of osteodystrophia fibrosa may develop
and distinction of the origin of these osteodystrophies based on only gross
and microscopic examination is impractical.
Differential diagnoses
A diagnosis of vitamin D deficiency depends upon evidence of the
probable occurrence of the deficiency and response of the animal when
vitamin D is provided.
Differentiation from clinically similar syndromes is discussed under the
specific osteodystrophies.
Treatment Administer vitamin D parent rally and oral calcium and
phosphates.
Control
Supplementation
The administration of supplementary vitamin D to animals by adding it to
the diet or by injection is necessary only when exposure to sunlight or the
provision of a natural ration containing adequate amounts of vitamin D is
impractical.
A total daily intake of 7-12 IU/kg BW is optimal. Sun-dried hay is a
good source, but green fodders are generally deficient in vitamin D.
Fish liver oils are high in vitamin D, but are subject to deterioration on
storage, particularly with regard to vitamin A. They have the added
disadvantage of losing their vitamin A and D content in premixed feed, of
destroying vitamin E in these feeds when they become rancid and of
seriously reducing the butterfat content of milk.
Irradiated dry yeast is probably a Simpler and cheaper method of
supplying vitamin D in mixed grain feeds.
Because there is limited storage of vitamin D in the body, compared to
the storage of vitamin A, it is recommended that daily dietary
supplementation be provided when possible for optimum effect.
Injection
In situations where dietary supplementation is not possible, the use of
single 1M injections of vitamin D2 (calciferol) in oil will protect
ruminants for 3-6 months. A dose of 11 000 units/kg BW is
recommended and should maintain an adequate vitamin D status for 3-6
months.
In mature non-pregnant sheep weighing about 50 kg, a single IM
injection of 6000 IU/kg body weight.
Rickets
Rickets is a disease of young, growing animals characterized by defective
calcification of growing bone. The essential lesion is a failure of
provisional calcification with persistence of hypertrophic cartilage and
enlargement of the epiphyses of long bones and the costochondral
junctions (so-called 'rachitic rosary) . The poorly mineralized
bones are subject to pressure distortions.
Etiology
Rickets is caused by an absolute or relative deficiency of any or a
combination of calcium, phosphorus, or vitamin D in young, growing
animals. The effects of the deficiency are also exacerbated by a rapid
growth rate.
An inherited form of rickets has been described in pigs. It is
indistinguishable from rickets caused by nutritional inadequacy.
Epidemiology
Rickets is a disease of young, rapidly growing animals and occurs
naturally under the following conditions.
Calves
Primary phosphorus deficiency in phosphorus- deficient range areas and
vitamin D deficiency in calves housed for long periods are the common
circumstances.
Vitamin D deficiency is the most common form of rickets in cattle raised
indoors for prolonged periods in Europe and North America. Grazing
animals may also develop vitamin D deficiency rickets at latitudes where
solar irradiation during winter is insufficient to promote adequate dermal
photobiosynthesis of vitamin D 3 from 7 -dihydrocholesterol. In young,
rapidly growing cattle raised intensively indoors a combined deficiency
of calcium, phosphorus and vitamin D can result in leg weakness
characterized by stiffness, reluctance to move, and retarded growth.
In some cases, rupture of the Achilles tendon and spontaneous fracture
occur.
Lambs
Lambs are less susceptible to primary phosphorus deficiency than cattle,
but rickets does occur under the same conditions. Green cereal grazing
and, to a lesser extent, pasturing on lush ryegrass during winter months
may cause a high incidence of rickets in lambs; this is considered to be a
secondary vitamin D deficiency.
An outbreak of vitamin D deficiency rickets involving 50% of lambs
aged 6-12 months grazing new grass and rape occurred during the early
winter months in Scotland.
Foals
Rickets is uncommon in foals under natural conditions, although it has
been produced experimentally.
Pathogenesis
Dietary deficiencies of calcium, phosphorus, and vitamin D result in
defective mineralization of the osteoid and cartilaginous matrix of
developing bone.
There is persistence and continued growth of hypertrophic epiphyseal
cartilage, increasing the width of the epiphyseal plate.
Poorly calcified spicules of diaphyseal bone and epiphyseal cartilage
yield to normal stresses, resulting in bowing of long bones and
broadening of the epiphyses with apparent enlargement of the joints.
Rapidly growing animals on an otherwise good diet will be first affected
because of their higher requirement of the specific nutrients.
Clinical findings
The subclinical effects of the particular deficiency disease will be
apparent in the group of animals affected and have been described in the
earlier general section.
Clinical rickets is characterized by:
1-Stiffness in the gait.
2- Enlargement of the limb joints, especially in the forelegs.
3- Enlargement of the costochondral junctions.
4-Long bones show abnormal curvature, usually forward and outward at
the carpus in sheep and cattle.
5- Lameness and a tendency to lie down for long periods.
6-Outbreaks affecting 50% of a group of lambs have been described.
Arching of the back and contraction, often to the point of virtual collapse,
of the pelvis occur and there is an increased tendency for bones to
fracture.
7-Eruption of the teeth is delayed and irregular, and the teeth are poorly
calcified with pitting, grooving, and pigmentation.
These dental abnormalities, together with thickening and softness of the
jaw bones, may make it impossible for severely affected calves and lambs
to close their mouths.
As a consequence, the tongue protrudes and there is drooling of saliva
and difficulty in feeding. In less severely affected animals, dental
malocclusion may be a significant occurrence.
8- Severe deformity of the chest may result in dyspnea and chronic
ruminal tympany.
9-In the final stages, the animal shows hypersensitivity; tetany,
recumbency and eventually dies of inanition.
D.D
Copper deficiency in young cattle under 1 year of age can also result in
clinical, radiographic and pathological findings similar to rickets.
Copper concentration in plasma and liver are low and there is usually
dietary evidence of copper deficiency.
Epiphysitis occurs in rapidly growing yearling cattle raised and fed
intensively under confinement. There is severe lameness, swelling of the
distal physes and radiographic and pathological evidence of a necrotizing
epiphysitis.
Congenital and acquired abnormalities of the bony skeletal system are
frequent in newborn and rapidly growing foals.
Mycoplasmal synovitis and arthritis
There is a sudden onset of stiffness of gait, habitual recumbence, a
decrease in feed consumption, and enlargements of the distal aspects of
the long bones which may or may not be painful, spontaneous recovery
usually occurs in 1 0-14 days.
Treatment and control
Recommendations for the treatment of the individual dietary deficiencies
(calcium, phosphorus and vitamin D) are presented under their respective
headings. Lesser deformities recover with suitable treatment but gross
deformities usually persist.
A general improvement in appetite and condition occurs quickly and is
accompanied by a return to normal blood levels of phosphorus and
alkaline phosphatase.
The treatment of rickets in lambs with vitamin A, vitamin D3, calcium
borogluconate solution containing magnesium and phosphorus
parenterally and supplementation of the diet with bone meal and protein
resulted in a dramatic response.
Osteomalacia
Osteomalacia is a disease of mature animals affecting bones in which
endochondral ossification has been completed.
The characteristic lesion is osteoporosis and the formation of excessive
un calcified matrix. Lameness and pathological fractures are the common
clinical findings.
Etiology
In general, the etiology and occurrence of osteomalacia are the same as
for rickets except that the predisposing cause is not the increased
requirement of growth but the drain of lactation and pregnancy.
Epidemiology Osteomalacia occurs in mature animals under the same
conditions and in the same areas as rickets in young animals, but is
recorded less commonly. Its main occurrence is in cattle in areas
seriously deficient in phosphorus. It is also recorded in sheep, again in
association with hypophosphatemia. In pastured animals, osteomalacia is
most common in cattle, and sheep raised in the same area are less
severely affected.
In feedlot animals, excessive phosphorus intake without complementary
calcium and vitamin D is likely as a cause, especially if the animals are
kept indoors. Intensively-fed yearling cattle with inadequate mineral
supplenlentation may be affected with spontaneous fractures of the
vertebral bodies, pelvic bones and long bones, leading to recumbency.
Pathogenesis
Increased re sorption of bone mineral to supply the needs of pregnancy,
lactation and endogenous metabolism leads to osteoporosis, and
weakness and deformity of the bones. Large amounts of uncalcified
osteoid are deposited about the diaphyses.
Pathological fractures are commonly precipitated by sudden exercise or
handling of the animal during transportation.
Clinical findings
Ruminants In the early stages, the signs are those of phosphorus
deficiency, including lowered productivity and fertility and loss of
condition.
Licking and chewing of inanimate objects begins at this stage and may
bring their attendant ills of oral, pharyngeal, and esophageal obstruction,
traumatic reticuloperitonitis, lead poisoning, and botulism.
The signs specific to osteomalacia are those of a painful condition of the
bones and joints and include a stiff gait, moderate lameness often shifting
from leg to leg, crackling sounds while walking, and an arched back.
The hind legs are most severely affected and the hocks may be rotated
inwards. The animals are disinclined to move, lie down for long periods
and are unwilling to get up.
The names 'milkleg' and 'milk-lameness' are commonly applied to the
condition when it occurs in heavily milking cows. Fractures of bones and
separation of tendon attachments occur frequently, often without apparent
precipitating stress.
In extreme cases, deformities of bones occur and when the pelvis is
affected dystocia may result.
Finally, weakness leads to permanent recumbencv and death from
starvation.
Clinical pathology
In general, the findings are the same as those for rickets, including
increased serum alkaline phosphatase and decreased serum phosphorus
levels. Radiographic examination of long bones shows decreased density
of bone shadow.
D.D
The occurrence of non-specific lameness with pathological fractures in
mature animals should arouse suspicion of osteomalacia. There may be
additional evidence of subnormal productivity and reproductive
performance and dietary evidence of a recent deficiency of calcium,
phosphorus, or vitamin D.
I n cattle it must be differentiated from chronic fluorosis in mature
animals, but the typical mottling and pitting of the teeth and the
enlargements on the shafts of the long bones are characteristic.
Treatment and control
Recommendations for the treatment and control of the specific nutritional
deficiencies have been described under their respective headings. Some
weeks will elapse before improvement occurs and deformities of the
bones are likely to be permanent.
Osteodystrophia fibrosa
Osteodystrophia fibrosa is similar in its pathogenesis to osteomalacia, but
differs in that soft, cellular, fibrous tissue is laid down as a result of the
weakness of the bones instead of the specialized uncalcified osteoid tissue
of osteomalacia. It occurs in horses, goats, and pigs.
Etiology
A secondary calcium deficiency due to excessive phosphorus feeding is
the common cause in horses and probably also in pigs.
Epidemiology
Osteodystrophia fibrosa is principally a disease of horses and other
Equidae and to a lesser extent of pigs. It has also occurred in goats.
Among horses, those engaged in heavy city work and in racing are more
likely to be affected because of the tendency to maintain these animals
on unbalanced diets. The major occurrence is in horses fed a diet high in
phosphorus and low in calcium. Such diets include cereal hays combined
with heavy grain or bran feeding. Legume hays, because of their high
calcium content, are preventive.
Pathogenesis
Defective mineralization of bones follows the imbalance of calcium and
phosphorus in the diet and a fibrous dysplasia occurs, This may be in
response to the weakness of the bones or it may be more precisely
a response to hyperparathyroidism stimulated by the excessive intake of
phosphorus.
The weakness of the bones predisposes to fractures and separation of
muscular and tendinous attachments. Articular erosions occur commonly
and displacement of the bone marrow may cause the development of
anemia.
Clinical findings
Horse
In horses, a shifting lameness is characteristic of this stage of the disease
and arching of the back may sometimes occur. The horse is lame, but
only mildly so and in many cases, no physical deformity can be found by
which the seat of lameness can be localized. Such horses often creak
badly in the joints when they walk. These signs probably result from
relaxation of tendon and ligaments and appear in different limbs at
different times. Articular erosions may contribute to the lameness,
In more advanced cases severe injuries, including fracture and visible
sprains of tendons, may occur. Fracture of the lumbar vertebrae while
racing has been known to occur in affected horses.
Flattening of the ribs may be apparent and fractures and detachment of
ligaments occur if the horse is worked, There may be obvious swelling of
joints and curvature of long bones, Severe emaciation and anemia occur
in the final stages,
Pigs
In pigs, the lesions and signs are similar to those in the horse and in
severe cases, pigs may be unable to rise and walk, show gross distortion
of limbs and enlargement of joints and the face. In less severe cases,
there is lameness, reluctance to rise, pain on standing and bending of the
limb bones, but normal facial bones and joints, With suitable treatment,
the lameness
Goats
Affected goats were 9-10 months of age with a history of stunted growth,
lameness, diarrhea, and tongue protrusion. Clinically there was
symmetrical enlargement of the face and jaws, tongue protrusion,
prominent eyeballs, and tremor. The enlarged bones were firm and
painful on palpation, The hind limbs were bent outwards symmetrically
from the tarsal joints,
Treatment and control
A ration adequately balanced with regard to calcium and phosphorus
(calcium: phosphorus should be in the vicinity of 1:1 and not wider than
1:1.4) is preventive in horses and affected animals can only be treated by
correcting the existing imbalance.
Even severe lesions may disappear in time with proper treatment. Cereal
hay maybe supplemented with alfalfa or clover hay, or finely ground
limestone (30 g daily) should be fed.